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Journal Abstract Search

214 related items for PubMed ID: 23744350

  • 1. Consequences of the combined loss of BOK and BAK or BOK and BAX.
    Ke F, Bouillet P, Kaufmann T, Strasser A, Kerr J, Voss AK.
    Cell Death Dis; 2013 Jun 06; 4(6):e650. PubMed ID: 23744350
    [Abstract] [Full Text] [Related]

  • 2. Embryogenesis and Adult Life in the Absence of Intrinsic Apoptosis Effectors BAX, BAK, and BOK.
    Ke FFS, Vanyai HK, Cowan AD, Delbridge ARD, Whitehead L, Grabow S, Czabotar PE, Voss AK, Strasser A.
    Cell; 2018 May 17; 173(5):1217-1230.e17. PubMed ID: 29775594
    [Abstract] [Full Text] [Related]

  • 3. Impact of the combined loss of BOK, BAX and BAK on the hematopoietic system is slightly more severe than compound loss of BAX and BAK.
    Ke F, Grabow S, Kelly GL, Lin A, O'Reilly LA, Strasser A.
    Cell Death Dis; 2015 Oct 22; 6(10):e1938. PubMed ID: 26492371
    [Abstract] [Full Text] [Related]

  • 4. Bok Is Not Pro-Apoptotic But Suppresses Poly ADP-Ribose Polymerase-Dependent Cell Death Pathways and Protects against Excitotoxic and Seizure-Induced Neuronal Injury.
    D'Orsi B, Engel T, Pfeiffer S, Nandi S, Kaufmann T, Henshall DC, Prehn JH.
    J Neurosci; 2016 Apr 20; 36(16):4564-78. PubMed ID: 27098698
    [Abstract] [Full Text] [Related]

  • 5. The BCL-2 family member BID plays a role during embryonic development in addition to its BH3-only protein function by acting in parallel to BAX, BAK and BOK.
    Ke FS, Holloway S, Uren RT, Wong AW, Little MH, Kluck RM, Voss AK, Strasser A.
    EMBO J; 2022 Aug 01; 41(15):e110300. PubMed ID: 35758142
    [Abstract] [Full Text] [Related]

  • 6. Bok is a genuine multi-BH-domain protein that triggers apoptosis in the absence of Bax and Bak.
    Einsele-Scholz S, Malmsheimer S, Bertram K, Stehle D, Johänning J, Manz M, Daniel PT, Gillissen BF, Schulze-Osthoff K, Essmann F.
    J Cell Sci; 2016 Jun 01; 129(11):2213-23. PubMed ID: 27076518
    [Abstract] [Full Text] [Related]

  • 7. Contribution of BH3-domain and Transmembrane-domain to the Activity and Interaction of the Pore-forming Bcl-2 Proteins Bok, Bak, and Bax.
    Stehle D, Grimm M, Einsele-Scholz S, Ladwig F, Johänning J, Fischer G, Gillissen B, Schulze-Osthoff K, Essmann F.
    Sci Rep; 2018 Aug 20; 8(1):12434. PubMed ID: 30127460
    [Abstract] [Full Text] [Related]

  • 8. Intracellular localization of the BCL-2 family member BOK and functional implications.
    Echeverry N, Bachmann D, Ke F, Strasser A, Simon HU, Kaufmann T.
    Cell Death Differ; 2013 Jun 20; 20(6):785-99. PubMed ID: 23429263
    [Abstract] [Full Text] [Related]

  • 9. BCL-2 family member BOK is widely expressed but its loss has only minimal impact in mice.
    Ke F, Voss A, Kerr JB, O'Reilly LA, Tai L, Echeverry N, Bouillet P, Strasser A, Kaufmann T.
    Cell Death Differ; 2012 Jun 20; 19(6):915-25. PubMed ID: 22281706
    [Abstract] [Full Text] [Related]

  • 10. Combined loss of proapoptotic genes Bak or Bax with Bim synergizes to cause defects in hematopoiesis and in thymocyte apoptosis.
    Hutcheson J, Scatizzi JC, Bickel E, Brown NJ, Bouillet P, Strasser A, Perlman H.
    J Exp Med; 2005 Jun 20; 201(12):1949-60. PubMed ID: 15967824
    [Abstract] [Full Text] [Related]

  • 11. Bax and Bak genes are essential for maximum apoptotic response by curcumin, a polyphenolic compound and cancer chemopreventive agent derived from turmeric, Curcuma longa.
    Shankar S, Srivastava RK.
    Carcinogenesis; 2007 Jun 20; 28(6):1277-86. PubMed ID: 17277231
    [Abstract] [Full Text] [Related]

  • 12. The Mysteries around the BCL-2 Family Member BOK.
    Shalaby R, Flores-Romero H, García-Sáez AJ.
    Biomolecules; 2020 Dec 04; 10(12):. PubMed ID: 33291826
    [Abstract] [Full Text] [Related]

  • 13. Raptinal bypasses BAX, BAK, and BOK for mitochondrial outer membrane permeabilization and intrinsic apoptosis.
    Heimer S, Knoll G, Schulze-Osthoff K, Ehrenschwender M.
    Cell Death Dis; 2019 Jul 19; 10(8):556. PubMed ID: 31324752
    [Abstract] [Full Text] [Related]

  • 14. Delayed-onset caspase-dependent massive hepatocyte apoptosis upon Fas activation in Bak/Bax-deficient mice.
    Hikita H, Takehara T, Kodama T, Shimizu S, Shigekawa M, Hosui A, Miyagi T, Tatsumi T, Ishida H, Li W, Kanto T, Hiramatsu N, Shimizu S, Tsujimoto Y, Hayashi N.
    Hepatology; 2011 Jul 19; 54(1):240-51. PubMed ID: 21425311
    [Abstract] [Full Text] [Related]

  • 15. Bok is a pro-apoptotic Bcl-2 protein with restricted expression in reproductive tissues and heterodimerizes with selective anti-apoptotic Bcl-2 family members.
    Hsu SY, Kaipia A, McGee E, Lomeli M, Hsueh AJ.
    Proc Natl Acad Sci U S A; 1997 Nov 11; 94(23):12401-6. PubMed ID: 9356461
    [Abstract] [Full Text] [Related]

  • 16. BCL-2 family member BOK promotes apoptosis in response to endoplasmic reticulum stress.
    Carpio MA, Michaud M, Zhou W, Fisher JK, Walensky LD, Katz SG.
    Proc Natl Acad Sci U S A; 2015 Jun 09; 112(23):7201-6. PubMed ID: 26015568
    [Abstract] [Full Text] [Related]

  • 17. Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule-specific knockout mouse models.
    Wei Q, Dong G, Chen JK, Ramesh G, Dong Z.
    Kidney Int; 2013 Jul 09; 84(1):138-48. PubMed ID: 23466994
    [Abstract] [Full Text] [Related]

  • 18. Pro-apoptotic Bax is the major and Bak an auxiliary effector in cytokine deprivation-induced mast cell apoptosis.
    Karlberg M, Ekoff M, Labi V, Strasser A, Huang D, Nilsson G.
    Cell Death Dis; 2010 May 13; 1(5):e43. PubMed ID: 21364649
    [Abstract] [Full Text] [Related]

  • 19. Proapoptotic bcl-2 family members, Bax and Bak, are essential for developmental photoreceptor apoptosis.
    Hahn P, Lindsten T, Ying GS, Bennett J, Milam AH, Thompson CB, Dunaief JL.
    Invest Ophthalmol Vis Sci; 2003 Aug 13; 44(8):3598-605. PubMed ID: 12882813
    [Abstract] [Full Text] [Related]

  • 20. Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins.
    Brooks C, Wei Q, Feng L, Dong G, Tao Y, Mei L, Xie ZJ, Dong Z.
    Proc Natl Acad Sci U S A; 2007 Jul 10; 104(28):11649-54. PubMed ID: 17606912
    [Abstract] [Full Text] [Related]

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